TY - JOUR
T1 - Ecm33 is a novel factor involved in efficient glucose uptake for nutrition-responsive TORC1 signaling in yeast
AU - Umekawa, Midori
AU - Ujihara, Masato
AU - Nakai, Daiki
AU - Takematsu, Hiromu
AU - Wakayama, Mamoru
N1 - Funding Information:
We thank Prof. Robbie Loewith (University of Geneva, Switzerland), Prof. Yoshiharu Inoue (Kyoto University, Japan) and Prof. Daniel J Klionsky (University of Michigan, USA) for generous gift of plasmids. We also thank Prof. Joerg Eichler (Elsevier, Germany) for editing the manuscript. This work was financially supported by JSPS KAKENHI No.25850246 (to MU) and No.17J40139 (to MU), and in part by Dr. Yoshifumi Jigami Memorial Fund No.203171500010, The Society of Yeast Scientists (to MU).
Publisher Copyright:
© 2017 Federation of European Biochemical Societies
PY - 2017/11
Y1 - 2017/11
N2 - Glucose uptake is crucial for providing both an energy source and a signal that regulates cell proliferation. Therefore, it is important to clarify the mechanisms underlying glucose uptake and its transmission to intracellular signaling pathways. In this study, we searched for a novel regulatory factor involved in glucose-induced signaling by using Saccharomyces cerevisiae as a eukaryotic model. Requirement of the extracellular protein Ecm33 in efficient glucose uptake and full activation of the nutrient-responsive TOR kinase complex 1 (TORC1) signaling pathway is shown. Cells lacking Ecm33 elicit a series of starvation-induced pathways even in the presence of extracellular high glucose concentration. This results in delayed cell proliferation, reduced ATP, induction of autophagy, and dephosphorylation of the TORC1 substrates Atg13 and Sch9.
AB - Glucose uptake is crucial for providing both an energy source and a signal that regulates cell proliferation. Therefore, it is important to clarify the mechanisms underlying glucose uptake and its transmission to intracellular signaling pathways. In this study, we searched for a novel regulatory factor involved in glucose-induced signaling by using Saccharomyces cerevisiae as a eukaryotic model. Requirement of the extracellular protein Ecm33 in efficient glucose uptake and full activation of the nutrient-responsive TOR kinase complex 1 (TORC1) signaling pathway is shown. Cells lacking Ecm33 elicit a series of starvation-induced pathways even in the presence of extracellular high glucose concentration. This results in delayed cell proliferation, reduced ATP, induction of autophagy, and dephosphorylation of the TORC1 substrates Atg13 and Sch9.
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U2 - 10.1002/1873-3468.12882
DO - 10.1002/1873-3468.12882
M3 - Article
C2 - 29029364
AN - SCOPUS:85035782884
VL - 591
SP - 3721
EP - 3729
JO - FEBS Letters
JF - FEBS Letters
SN - 0014-5793
IS - 22
ER -